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Updated: Jun 21, 2026

Computational Prediction of Amino Acid Preferences of Potentially Multispecific Peptide-Binding Domains Involved in Protein-Protein Interactions
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Generating models for isoform-specific PKM-KIBRA interactions with BIFC, stabilization and AlphaFold 3.

Edna Amoah1, Tyler W Dunn1, Larissa Ferguson1

  • 1Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, QC, H3A 2B4, Canada.

Molecular Brain
|June 19, 2026
PubMed
Summary
This summary is machine-generated.

Aplysia Kidney/Brain protein (KIBRA) interactions with protein kinase M (PKM) variants were studied. Some KIBRA variants bind PKM but do not stabilize it, suggesting inhibition is key for memory maintenance.

Keywords:
Atypical protein kinase CMemory retentionPKCPersistent protein kinasesProtein complexesSynaptic plasticity

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Protein kinase M (PKM) is crucial for long-term memory.
  • Aplysia Kidney/Brain protein (KIBRA) stabilizes atypical PKM Apl III.
  • KIBRA variants affect PKM stabilization and neuronal plasticity.

Purpose of the Study:

  • Investigate biomolecular fluorescence complementation (BIFC) between KIBRA variants and PKM Apl III.
  • Examine KIBRA variants with altered binding sites and mutations.
  • Understand the discrepancy between KIBRA-PKM binding and PKM stabilization.

Main Methods:

  • Biomolecular fluorescence complementation (BIFC) in Aplysia neurons.
  • Analysis of KIBRA variants with modified binding sites.
  • Utilizing AlphaFold 3 for protein-protein interaction modeling.

Main Results:

  • Some KIBRA variants exhibit BIFC with PKM Apl III without stabilizing it.
  • Altered KIBRA binding sites disrupt PKM Apl III stabilization and plasticity.
  • Protein interaction modeling provided insights into BIFC-stabilization discrepancies.

Conclusions:

  • KIBRA-PKM interaction does not always equate to stabilization.
  • Stable inhibition of PKM by KIBRA may be essential for memory maintenance.
  • Further research into KIBRA's inhibitory role in PKM regulation is warranted.